During the past two decades, infrared radiation has received much less attention than ultraviolet with respect to its cutaneous effects. Infrared photons (appreciated by the average human as a sensation of heat) are of relatively low energy. Hence, it has been stated that the inability to start photochemical reactions mitigates infrared's possible contributions to cutaneous carcinogenesis. Only recently has it been suspected that this old view might be fallacious since biochemical reactions are heat-dependent:
-DG.degree.=RT in K (where DG is the standard free energy, R is the gas constant and K is the equilibrium constant).
It is now believed that the infrared/heat axis may contribute to aging and carcinogenesis by amplifying ultraviolet injury, altering the vasculature, producing diffusible mediators, changing histone binding properties, and/or damaging DNA repair processes. (See: Kaidbey, et al, Arch. Dermatol., 1982; 118 (5):315-318.)
Present sunscreens protect against ultraviolet UVB and UVA. Unfortunately, they are no more effective than most types of glass at absorbing infrared radiation. (See: O'Brien, J. P., Austral J. Dermatol., 1980; 21: 1-9.) Infrared rays penetrate deeper than UV rays, and, once absorbed, propagate heat further by conduction and convection. (See: O'Brien, J.P., Arch. Dermatol., 1975; 111: 460-466.) Therefore, present sunscreens leave the skin naked to the atmospherically transmitted infrared radiation. Absorbance and reflectance data have been generated for human skin both white and black, over the 0.4 to 1.6 m (micron) range. The reflectance curves above 1.2 m for differently pigmented persons are practically identical and reflect primarily the absorption spectrum of water. In the spectral range 0.4 m, the reflectance is usually between 50%-70% (the absorbance decreasing as the reflectance increases, indicating relative translucency). Between 0.7 and 2.6 m, water causes prominent absorption bands. This results in reflectance of only 10% from 1.4 m out to 2.6 m. These values are pertinent, especially in high atmospheric transmission wavelengths. (See: Jaquez, J. A. et al., J. Appl. Physiol., 1955; 8: 297-299; and Kuppenheim, H. F. et al., J. Appl. Physiol., 1955; 9: 75-78.)
Principal considerations for selecting effective sunscreens include burning, tanning, and chronic changes such as, cancer, elastosis, wrinkling, telangiectasias and pigmentary mottling. When considering the need for infrared protection, however, little information is available.
Some conditions exist which appear to be associated "purely" with heat or infrared radiation, such as, cutis laxa, that is wizened skin of certain glass blowers, kitchen workers, bakers working with space heating devices (whose biopsies show elastosis); "Glass makers" cataract; Kang cancer of northern China (induced by sleeping on hot bricks); Kangri cancer of India (induced by wearing coal burning pots); Kairo cancer of Japan (from wearing benzene burning flasks); Peat fire cancer of Irish women; and basal cell tumors of cheeks induced by the solar focusing of rimless glasses.
Other diaseases associated with infrared exposure include temporal arteritis and actinic granuloma. (See: O'Brien, op cit; and Shabrad, P. et al., Br. J. Dermatol., 1977; 97: 179-186.) In many of these entities, the cutaneous malignancies were found among the clinical changes of erythema ag igne. According to Kligman "whether heat reaches the skin by conduction (i.e., hot bricks, heating pads) or by radiation (i.e., open fires, space heaters), the changes are quite similar. Cancers and erythema ab igne can be produced by either route. (See: "Reflections on Heat", Br. J. Dermatol, 1984; 110: 369-355.) The possibility of erythema ab igne being a marker for infrared damage and a predictor for later skin cancers is recognized.
Histologically, similarities between chronic actinic damage and erythema ab igne from non-burning infrared include: early elastic fiber proliferation, increased dermal mast cells, telangiectasia, epidermal dysplasia, and atypia, and irregular melanin distribution. Dissimilarities include greater dermal melanin or hemosiderin deposition and less end-stage degenerative elastosis found in erythema ab igne. The mild upper dermal elastosis of erythema ab igne is superficial. This elastotic material histochemically approximates hyaluronic acid. Epidermal changes of erythema ab igne include atypia amounting to preneoplatic change and basal cell vacuolization. These effects may possibly be caused by infrared radiation, since heat has been shown to cause: cellular respiratory inhibition; decreased DNA, RNA, and protein macromolecular synthesis; increased cellular membrane permeability; decreased nucleolar-cytoplasmic transport of ribosomal RNA; and G.sub.2 cell cycle phase accumulations.
Actinic elastosis has been claimed "the chief component if not the basis of aging in sun exposed skin. Also, elastosis is more prominent on biopsy than is clinically apparent." Since elastosis may be unsightly (yellow, wrinkles), preventing infrared or ultraviolet induced elastosis would be a major benefit.
At present, no direct clinical studies adequately separate solar elastosis into ultraviolet versus infrared components, and their respective proportions in humans. Finlayson's work on erythema ab igne indicates only that infrared radiation can cause elastosis in humans. (See: "Erythema ab igne: A histopathological study". J. Invest. Dermatol., 1966; 46: 104-108.) Kligman showed, using guinea pigs, that ultraviolet radiation, alone, produced more numerous, thicker, twisted elastic fibers. Physiologic range infrared radiation, alone, produced numerous fine, feather-like fibers. Infrared and ultraviolet radiations simultaneously produced dense mat-like fibers and increased ground substance that exceeded the sole product of either radiation alone.
The argument has been made that actinic elastosis can be minimized by the use of present ultraviolet sunscreens. An opposing opinion was presented by Pearse, who implied that ultraviolet protection does not insure against chronic sun damage. Some believe that solar elastosis is the result of damaged fibroblasts secreting defective proteins. Infrared radiation has been shown to alter some cellular proteins (enzymes). Further studies are required to determine if infrared radiation affects enzymes or other proteins necessary to the manufacture of elastin.
A dramatic example of solar elastosis may effect the temporal arteries. A study by O'Brien (Op. cit.) reported that the outermost side of temporal arteries possesses the actinic damage similar in severity to exposed skin. Theoretically, only infrared radiation should penetrate to this depth.
Perhaps a better way to separate ultraviolet and infrared effects is through study of the black patient. The black individual, in comparison with the white, is relatively ultraviolet A and B resistant. Black skin, however, has greater infrared and visible radiation absorption. Kligman and Kligman believe that "much of the elastosis in blacks is due to infrared radiation alone." This should be tempered by the fact that, of all racial groups, blacks have the least (highest resistance to) elastosis.
A unique line of reasoning implicates infrared radiation as the cause of actinic granuloma. Nigerians have a 1.7% prevalence of extremely rare granuloma multiforme, the Nigerian equivalent of actinic granuloma. Alledgedly, these Nigerians differ from other blacks because they are exposed to much domestic fire radiation. Therefore, fire exposure, providing infrared radiation and convection heat, is implicated as a cause of actinic granuloma, an elastolytic condition.
The study of the individual effects of infrared or ultraviolet radiation alone may have scholarly merit; but the combination of ultraviolet and infrared radiation may have the greatest effects. Again, heat has been shown to decrease DNA repair after ionizing radiation.
In a more applicable vein, ultraviolet and heat have been shown to synergistically denature human squamous buccal mucosal DNA. This work was carried out at 24.degree. C., 32.degree. C. (representing the temperature of indoor surface skin), and 42.degree. C. (representing the surface skin temperature in bright sunlight at 26.degree. North latitude). (See: Roth and London: J. Investigative Dermatology; 69, 368-372; 1977.) Roth et al showed a positive linear relationship between DNA denaturation and irradiation temperature.
In a classic study, Freeman and Knox (See: Archives of Dermatology; 89, 858-64; 1964) showed that acute, as well as chronic, combined ultraviolet and infrared exposures may have deleterious effects on mouse skin. The mouse acute-ultraviolet-burn-death-rate rose with temperature. The greatest percentages of mouse cutaneous tumors resulted from ultraviolet exposure and continuous heat as opposed to all other groups to be mentioned. Heat, delivered for three hours following a daily ultraviolet dose, resulted in a greater tumor yield than heat delivered in the immediate three hours prior to the ultraviolet treatment. All of the aforementioned tumor yields were greater than in mice given ultraviolet therapy without exogenous heat.
While more studies may be considered necessary such as, for example, the monitoring of subjects located in variable latitudes and insolation, for both ultraviolet and infrared in regard to chronic deleterious solar effects, and biopsied, assessing one variable (i.e., infrared or ultraviolet) while holding the others constant to assess relative effects, there is sufficient evidence to give reasonable men concern that infrared is the source of deleterious cutaneous effects in man and to inspire efforts toward the development of topical preparations which can provide more than a modicum of protection of the human animal, irrespective of race or pigmentation.